Intrathecal Administration of Antibodies against LFA-1 and against ICAM-1 Suppresses Experimental Allergic Encephalomyelitis in Rats

Kawai, K; Kobayashi, Yasushi; Shiratori, Masayuki; Sobue, Gen; Tamatani, Takuya; Miyasaka, Masayuki; Yoshikai, Yasunobu

doi:10.1006/cimm.1996.0202

Cited by 42 publications

(24 citation statements)

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“…The results of this study clearly demonstrate that ICAM-1 plays a central role in the development of demyelinating disease. Our findings contrast with several previous EAE studies using inhibitory anti-ICAM-1 Abs or Icam1 tm1Bay mice (25)(26)(27)(28)(29)(30)(31). At least for the Ab studies, these contrasting findings may be due to a number of reasons, including differential Ab specificity, insufficient dosage, differences in the timing of Ab delivery, and methodological differences in the induction or characterization of EAE.…”

Section: Discussioncontrasting

confidence: 99%

“…The results we report here demonstrate that ICAM-1 is essential for the development of EAE and we would argue that it plays a similar role in MS. Therapeutic approaches to demyelinating disease in animal models and humans have focused primarily on inhibition of ␣ 4 integrins and LFA-1 (26,28,(47)(48)(49)(50). Our results argue that inhibitory approaches blocking ICAM-1-mediated functions warrant significant investigation in MS. Support for this argument comes from a recent study in which EAE was inhibited by treatment with a Staphylococcus aureus, extracellular adherence protein which binds to ICAM-1 (51).…”

Section: Discussionmentioning

confidence: 87%

“…Most reports have described results using inhibitory ICAM-1 mAbs to block interactions of this adhesion molecule with its ligands. Although several of these studies have shown a protective outcome in active EAE (25)(26)(27), an almost equal number have reported no protection or increased severity of disease (28 -30). In contrast, loss, or inhibition of the ICAM-1 ligands LFA-1 and Mac-1 in EAE models have, in most cases, shown reduction in clinical severity and partial protection against the development of CNS inflammation.…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

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Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Bullard¹,

Hu²,

Schoeb³

et al. 2007

The Journal of Immunology

125

103

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Many members of the Ig superfamily of adhesion molecules, such as ICAM-1 and VCAM-1, have been implicated in the pathogenesis of multiple sclerosis. Although it is well-established that VCAM-1/VLA-4 interactions can play important roles in mediating CNS inflammatory events in multiple sclerosis patients and during the development of experimental allergic encephalomyelitis (EAE), the contributions of ICAM-1 are poorly understood. This is due in large part to conflicting results from Ab inhibition studies and the observation of exacerbated EAE in ICAM-1 mutant mice that express a restricted set of ICAM-1 isoforms. To determine ICAM-1-mediated mechanisms in EAE, we analyzed ICAM-1 null mutant mice (ICAM-1null), which express no ICAM-1 isoforms. ICAM-1null mice had significantly attenuated EAE characterized by markedly reduced spinal cord T cell infiltration and IFN-γ production by these cells. Adoptive transfer of Ag-restimulated T cells from wild-type to ICAM-1null mice or transfer of ICAM-1null Ag-restimulated T cells to control mice failed to induce EAE. ICAM-1null T cells also showed reduced proliferative capacity and substantially reduced levels of IFN-γ, TNF-α, IL-4, IL-10, and IL-12 compared with that of control T cells following myelin oligodendrocyte glycoprotein 35–55 restimulation in vitro. Our results indicate that ICAM-1 expression is critical on T cells and other cell types for the development of demyelinating disease and suggest that expression of VCAM-1 and other adhesion molecules cannot fully compensate for the loss of ICAM-1 during EAE development.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 87%

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

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Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Bullard¹,

Hu²,

Schoeb³

et al. 2007

The Journal of Immunology

125

103

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“…Indeed, a number of laboratories have successfully employed antibodies directed at either endothelial adhesion molecules or their counter-receptors on leukocytes to lessen the severity and/or frequency of inflammatory episodes in EAE (Archelos et al, 1993;Huitinga et al, 1993;Gordon et al, 1995;Kawai et al, 1996;Leger et al, 1997;Rose et al, 1997;Soilu-Hanninen et al, 1997). As these endothelial/leukocyte interactions are not peculiar to the CNS and are vital to host-defense mechanisms, generalized immunologic blockades of this sort pose problems for long-term treatment of chronic CNS inflammatory disease in humans.…”

Section: Endothelial Cells As Therapeutic Targets and Effectors In Cnmentioning

confidence: 99%

Central nervous system endothelium in neuroinflammatory, neuroinfectious, and neurodegenerative disease

Andjelkovic

Pachter

1998

J. Neurosci. Res.

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“…Antibodies to ICAM-1 (Archelos et al, 1993;Kobayashi et al, 1995;Kawai et al, 1996;Morrissey et al, 1996) or to a4ßl (Yednock et al, 1992) have been shown to lessen the severity of EAE. Treatment of Lewis rats with antibody to ICAM-1 resulted in a reduced severity of EAE that was associated with diminished infiltration of leukocytes into the CNS (Archelos et al, 1993;Morrissey et al, 1996).…”

mentioning

confidence: 99%

Elevation of Cyclic AMP Levels in Astrocytes Antagonizes Cytokine‐Induced Adhesion Molecule Expression

Ballestas

Benveniste

1997

Journal of Neurochemistry

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Abstract:We have examined the effect of elevating cyclic AMP levels on cytokine-mediated enhancement of intercellular adhesion molecule-i (ICAM-i) and vascular cell adhesion molecule-i (VCAM-i) gene expression by astrocytes. Treatment of astrocytes with the cyclic AMP mimetic dibutyryl-cyclic AMP, or the agonists norepinephrine, forskolin, prostaglandin E 2, and cholera toxin alone had no effect on ICAM-i or VCAM-i mRNA gene expression. However, elevating cyclic AMP levels within the cells by these agents suppressed interleukin-i ß-and tumor necrosis factor-a-induced adhesion molecule expression at both the mRNA and protein levels. The phosphodiesterase type IV inhibitor, rolipram, was able to potentiate the inhibitory effect of forskolin on ICAM-i and VCAM-i gene expression. Inhibition of tumor necrosis factor-a-induced VCAM-i mRNA levels by forskolin was partially due to enhanced degradation of VCAM-i message, whereas the decay rates of tumor necrosis factora-induced ICAM-i message and interleukin-iß-induced ICAM-i /VCAM-i message were not affected by forskolin treatment. These results demonstrate that the pathways used by interleukin-iß and tumor necrosis factor-a to induce adhesion molecule expression are antagonized by cyclic AMP-dependent protein kinase-mediated signaling pathways.

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Intrathecal Administration of Antibodies against LFA-1 and against ICAM-1 Suppresses Experimental Allergic Encephalomyelitis in Rats

Cited by 42 publications

References 0 publications

Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Central nervous system endothelium in neuroinflammatory, neuroinfectious, and neurodegenerative disease

Elevation of Cyclic AMP Levels in Astrocytes Antagonizes Cytokine‐Induced Adhesion Molecule Expression

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